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. 2022 Apr 19;13:2022. doi: 10.1038/s41467-022-29701-x

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — A Principal Component Analysis of Rbpj^ΔEC vs. Control kidney EC transcription analysis, n = 3/group, (Variance filtering 0.05, Student’s T test followed by the B-H correction (p < 0.02, FDR < 0.0199731) showing biological replicates of each group clustering together (370 genes) (more information in “Methods”). B GO-term GSEA—selected significantly up- (red) and downregulated (blue) gene sets sorted by normalized enrichment score (NES). C Volcano plots of individual genes with expression changed in Rbpj^ΔEC compared to control, with log₂ (fold change) on x-axis and –log₁₀ (adjusted p-value) on the y-axis; in red, genes belonging to selected marker gene sets for different kidney arterial segments (from refs. ^49,50). NES and p value upper right corners; see “Methods” (GSEA) for statistics. D Homeostatic HEC marker gene set from¹² in red in same volcano plot, NES and p value upper right corner. See Methods (GSEA) for statistics. E Human kidney biopsy RNAseq (GSE: EC Notch target genes in different glomerular diseases downregulated as compared to living kidney donor biopsies as control. Abbreviations and sample number: LD, living kidney donor (n = 21); MemGN, membranous glomerulonephritis (n = 18); FSGS, focal segmental glomerulosclerosis (n = 17); MCD, minimal change disease(n = 13); RPGN, rapid-progressive glomerulonephritis (n = 21); IgA, Iga-Nephritis (n = 25); SLE, systemic lupus erythematodes (n = 32). Single samples (dot) plus mean, IQR (box) and total range (min-max: whiskers). Statistic: Brown-Forsythe and Welch (1 way) ANOVA with Dunnet’s multiple comparisons; exact adjusted p-values: HES1, compared to LD: MemGN <0.0001; FSGS, 0.068; MCD, <0.0001; RPGN, 0.0003; IgA, 0.0035; SLE, 0.0347. HEY1, compared to LD: MemGN, 0.3236; FSGS, 0.0076; MCD; 0.5432; RPGN, 0.1433; IgA, 0.5891; SLE, 0.9987. HEYL, compared to LD: MemGN, 0.119; FSGS, 0.002; MCD, 0.0050; RPGN, < 0.0001; IgA, 0.0085; SLE, 0.0021. Source data are provided as supplementary files.